Background Dysfunction in the ventromedial prefrontal cortex (vmPFC) is believed to play a
pivotal role in the pathogenesis of mood and anxiety disorders. Leading neurocircuitry
models of these disorders propose that hypoactivity in the vmPFC engenders disinhibited
activity of the amygdala and, consequently, pathologically elevated levels of negative affect.
This model predicts that a selective loss or diminution of function of the vmPFC would result
in heightened activity of the amygdala. Although this prediction has been borne out in rodent …